Mechanisms of nasal high flow on ventilation during wakefulness and sleep

Abstract

Nasal high flow (NHF) has been shown to increase expiratory pressure and reduce respiratory rate but the mechanisms involved remain unclear. Ten healthy participants [age, 22 ± 2 yr; body mass index (BMI), 24 ± 2 kg/m(2)] were recruited to determine ventilatory responses to NHF of air at 37°C and fully saturated with water. We conducted a randomized, controlled, cross-over study consisting of four separate ∼60-min visits, each 1 wk apart, to determine the effect of NHF on ventilation during wakefulness (NHF at 0, 15, 30, and 45 liters/min) and sleep (NHF at 0, 15, and 30 liters/min). In addition, a nasal cavity model was used to compare pressure/air-flow relationships of NHF and continuous positive airway pressure (CPAP) throughout simulated breathing. During wakefulness, NHF led to an increase in tidal volume from 0.7 ± 0.1 liter to 0.8 ± 0.2, 1.0 ± 0.2, and 1.3 ± 0.2 liters, and a reduction in respiratory rate (fR) from 16 ± 2 to 13 ± 3, 10 ± 3, and 8 ± 3 breaths/min (baseline to 15, 30, and 45 liters/min NHF, respectively; P < 0.01). In contrast, during sleep, NHF led to a ∼20% fall in minute ventilation due to a decrease in tidal volume and no change in fR. In the nasal cavity model, NHF increased expiratory but decreased inspiratory resistance depending on both the cannula size and the expiratory flow rate. The mechanisms of action for NHF differ from those of CPAP and are sleep/wake-state dependent. NHF may be utilized to increase tidal breathing during wakefulness and to relieve respiratory loads during sleep.

Figures

Fig. 1.

Illustration of nasal high-flow system and nasal cannula used in this study.

Fig. 2.

Representative 2-min trace from one subject illustrating tidal volume (VT) at baseline (top) and against NHF at control, 15, 30, and 45 liters/min (bottom).

Fig. 3.

Individual and mean (± SD) data for respiratory rate (fR, top) and tidal volume (VT, bottom) at baseline and following NHF at 15, 30, and 45 liters/min. *P < 0.05, **P < 0.01, and ***P < 0.001 indicate significant differences between control, no NHF, and intervention.

Fig. 4.

Individual and mean data for ventilatory responses during wakefulness (top) and sleep (bottom) in a subset of 3 individuals at baseline and following NHF at 15 and 30 liters/min.

Fig. 5.

Representative ∼10-min trace from one individual during non-rapid-eye movement stage N3 sleep illustrating a reduction in tidal volume [VT(RIP)], stable oxyhemoglobin, and reduced respiratory effort with NHF at 15 liters/min compared with baseline.

Fig. 6.

Experimental setup for experiments with the nasal cavity model. A: two streams of air, one bidirectional flow at the inlet was varied in 5 liters/min increments from −35 to +35 liters/min, simulating inspiratory and expiratory phases, respectively, and another unidirectional NHF jet, fixed at 15 liters/min, were generated and delivered at the outlet of the nasal cavity model through inelastic tubes (22- to 9.6-mm opening for variable flow and 6-mm for the jet) with rigid walls. B: pressure/air-flow relationship of NHF compared with control (open outlet) and CPAP.